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Article: Interleukin-4 gene expression in mercury-induced autoimmunity

TitleInterleukin-4 gene expression in mercury-induced autoimmunity
Authors
Issue Date1995
Citation
Scandinavian Journal of Immunology, 1995, v. 41 n. 3, p. 268-272 How to Cite?
AbstractMercuric chloride (HgCl2) induces autoimmunity in Brown Norway (BN) rats, with necrotizing vasculitis in the gut. Circumstantial evidence implicates the T(h)2 subset of CD4+ T lymphocytes, which produces IL-4. We developed a quantitative polymerase chain reaction (PCR) technique to quantify IL-4 gene expression. A phagemid containing rat IL-4 cDNA was modified to act as the template for a synthetic RNA construct; a known amount of synthetic RNA was added to total RNA from spleen and caecum of BN rats at various times after HgCl2, followed by reverse transcriptase PCR. IL-4 gene expression increased markedly in spleen and caecum after HgCl2. Splenic levels peaked by 10 days at approximately five-times baseline, then returned towards normal as the autoimmune response was spontaneously regulated. Caecal IL-4 expression peaked at 48 h, at which time we observed a previously unreported early phase of tissue injury, with necrotizing vasculitis qualitatively similar to that reported previously in the later phases of the model. These data support a key role for IL-4 in this experimental model of autoimmunity. The quantitative PCR technique can be modified for analysis of other cytokines, allowing further investigation of the role of T cell subsets in this model.
Persistent Identifierhttp://hdl.handle.net/10722/195333
ISSN
2015 Impact Factor: 2.27
2015 SCImago Journal Rankings: 0.934
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorGillespie, KM-
dc.contributor.authorQasim, FJ-
dc.contributor.authorTibbatts, LM-
dc.contributor.authorThiru, S-
dc.contributor.authorOliveira, DBG-
dc.contributor.authorMathieson, PW-
dc.date.accessioned2014-02-28T06:12:00Z-
dc.date.available2014-02-28T06:12:00Z-
dc.date.issued1995-
dc.identifier.citationScandinavian Journal of Immunology, 1995, v. 41 n. 3, p. 268-272-
dc.identifier.issn0300-9475-
dc.identifier.urihttp://hdl.handle.net/10722/195333-
dc.description.abstractMercuric chloride (HgCl2) induces autoimmunity in Brown Norway (BN) rats, with necrotizing vasculitis in the gut. Circumstantial evidence implicates the T(h)2 subset of CD4+ T lymphocytes, which produces IL-4. We developed a quantitative polymerase chain reaction (PCR) technique to quantify IL-4 gene expression. A phagemid containing rat IL-4 cDNA was modified to act as the template for a synthetic RNA construct; a known amount of synthetic RNA was added to total RNA from spleen and caecum of BN rats at various times after HgCl2, followed by reverse transcriptase PCR. IL-4 gene expression increased markedly in spleen and caecum after HgCl2. Splenic levels peaked by 10 days at approximately five-times baseline, then returned towards normal as the autoimmune response was spontaneously regulated. Caecal IL-4 expression peaked at 48 h, at which time we observed a previously unreported early phase of tissue injury, with necrotizing vasculitis qualitatively similar to that reported previously in the later phases of the model. These data support a key role for IL-4 in this experimental model of autoimmunity. The quantitative PCR technique can be modified for analysis of other cytokines, allowing further investigation of the role of T cell subsets in this model.-
dc.languageeng-
dc.relation.ispartofScandinavian Journal of Immunology-
dc.titleInterleukin-4 gene expression in mercury-induced autoimmunity-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/j.1365-3083.1995.tb03563.x-
dc.identifier.pmid7871386-
dc.identifier.scopuseid_2-s2.0-0028960808-
dc.identifier.volume41-
dc.identifier.issue3-
dc.identifier.spage268-
dc.identifier.epage272-
dc.identifier.isiWOS:A1995QK50600008-

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